| DBH | Dopamine-Beta(β)-Hydroxylase |
|---|---|
| BAI | basilar artery insufficiency; beta-aminoisobutyrate |
| BAIB | beta-aminoisobutyric [acid] |
| BAP | bacterial alkaline phosphatase; Behavior Activity Profile; beta-amyloid peptide; blood-agar plate; b... |
| BAPN | beta-aminoproprionitrile fumarate |
| genes, viral | The hereditary material of viruses, consisting in all DNA and some RNA viruses of a single molecule of nucleic acid, and in some RNA viruses of several separate pieces of RNA. (12 Dec 1998) |
|---|---|
| genes, vpr | DNA sequences that form the coding region for a trans-activator protein that specifies rapid growth in human immunodeficiency virus (HIV). Vpr is short for viral protein r, where r is undefined. (12 Dec 1998) |
| genes, vpu | DNA sequences that form the coding region for the HIV-1 regulatory protein vpu (viral protein u) that greatly increases the export of virus particles from infected cells. The vpu genes are not present in HIV-2 or siv. (12 Dec 1998) |
| genes, wilms' tumour | Tumour suppressor genes located in the 11p13 region on the short arm of human chromosome 11. The absence of these genes is associated with the formation of wilms' tumour. (12 Dec 1998) |
| VH and VL genes/domains | VH and VL genes define in part the sequences of the variable heavy and light regions of immunoglobulin molecules. VH and VL domains are the regions of amino acid sequence so defined. J genes and, in the case of the heavy chain, a D gene (D=diversity) also define these regions. Gene rearrangement also plays a role in determining the sequences in which the genes are joined as the DNA of the immunoglobulin producing cell matures. (18 Nov 1997) |
| mimic genes | Nonallelic (independent) gene's with closely similar effects, e.g., elliptocytosis. (05 Mar 2000) |
| homeotic genes | A group of genes that regulate the development of the body parts by defining the boundaries of the several regions. (05 Mar 2000) |
| housekeeping genes | Genes that are generally always expressed and thought to be involved in routine cellular metabolism. (05 Mar 2000) |
| SOS genes | A group of genes involved in DNA repair, often induced by damage severe enough to cause stoppage of DNA synthesis. (05 Mar 2000) |
| split genes | Genes where the genomic sequences are interrupted by intervening sequences (introns) that are spliced out of the mRNA prior to translation. (05 Mar 2000) |
| immune response genes | Gene's in the HLA-D region of the histocompatibility complex of human chromosome 6 which control the immune response to specific antigens. (05 Mar 2000) |
| transfer genes | Gene's carried by a conjugative plasmid, essential for fertility and establishment of the bacterial donor state. (05 Mar 2000) |
| acetylcholine receptor antibodies | <neurology, investigation> A test used to measure the amount of antibodies to acetylcholine receptors on nerve endings. This is a diagnostic test for myasthenia gravis. A normal value is no antibodies in the bloodstream. Acetylcholine receptor (AChR) binding autoantibodies (i.e. Antibodies reactive with several epitopes other than the binding site for acetylcholine or alpha-bungarotoxin) are present in approximately 88% of patients with generalised myasthenia gravis, 70% of ocular myasthenia and in approximately 80% of myasthenia gravis in remission. Although serum concentrations of AChR binding autoantibodies do not in general correlate well with severity of weakness, there is typical decrease in concentration as weakness improves with immunosuppressive therapy. AChR blocking autoantibodies (i.e., antibodies reactive with the AChR binding site) are present in about 50% of patients with myasthenia gravis, 30% with ocular myasthenia gravis and 20% of myasthenia gravis in remission, AChR blocking autoantibodies are the only AChR autoantibodies present in about 1% of myasthenia gravis. AChR modulating autoantibodies (i.e., autoantibodies which cross-link AChRs and cause their removal from muscle membrane surfaces) are present in more than 90% of myasthenia gravis and occasionally are the only AchR autoantibodies detectable in mild, recent onset or ocular-restricted myasthenia gravis. Results for AChR modulating autoantibodies can be transiently false-positive due to curare-like drugs used during general anesthesia. AChR autoantibodies of one or more types are found in at least 80% of ocular myasthenia gravis. Although generally absent in neurological conditions other than myasthenia gravis(and consequently unlikely to cause confusion in neurodiagnosis), false-positive results for AChR autoantibodies occasionally occur in primary biliary cirrhosis, tardive dyskinesia, autoimmune thyroiditis, the elderly, amyotrophic lateral sclerosis patients treated with cobra venom and patients with thymoma in the absence of myasthenia gravis. Approximately 1% of patients with rheumatoid arthritis treated with D-penicillamine develop AChR autoantibodies and myasthenia gravis, both of which disappear when the drug is discontinued. Babies born to ~10% of myasthenia gravis mothers have a transient neonatal form of myasthenia gravis that responds well to anticholinesterase therapy and usually remits within 1 month as maternal IgG disappears. (29 Dec 1997) |
| amino acid receptor | <biochemistry> Ligand gated ion channels with specific receptors for amino acid transmitters. An extended protein superfamily that also includes subunits of the nicotinic acetylcholine receptor. (18 Nov 1997) |
| AMPA receptor | <cell biology> Glutamate operated ion channel. See: excitatory amino acid receptor channels. (05 Feb 1998) |